ArticleBlood2006
Enhancement of infectivity and persistence in vivo by HBZ, a natural antisense coded protein of HTLV-1.
Article in Blood, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 123 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
123 citing papers in PubMed, 191 citations in OpenAlex.
- Systems biology approaches reveal a specific interferon-inducible signature in HTLV-1 associated myelopathy.PLoS pathogens · 2012Trial
- Splicing-dependent restriction of the HBZ gene by Tax underlies biphasic HTLV-1 infection.PLoS pathogens · 2025Article
- HTLV-I Basic Leucine Zipper Factor (sHBZ) Actively Associates with Nucleophosmin (B23) in the Nucleolus.Viruses · 2025Article
- YTHDF1 and YTHDC1 mJournal of virology · 2025Article
- Current State of Therapeutics for HTLV-1.Viruses · 2024Review
- High level of genomic divergence in orf-I p12 and hbz genes of HTLV-1 subtype-C in Central Australia.Retrovirology · 2024Article
- An HTLV-1 envelope mRNA vaccine is immunogenic and protective in New Zealand rabbits.Journal of virology · 2024Article
- Human T-Cell Leukemia Virus Type 1 Oncogenesis between Active Expression and Latency: A Possible Source for the Development of Therapeutic Targets.International journal of molecular sciences · 2023Review
- The Pleiotropic Effects of YBX1 on HTLV-1 Transcription.International journal of molecular sciences · 2023Article
- HTLV-1 Hbz protein, but not hbz mRNA secondary structure, is critical for viral persistence and disease development.PLoS pathogens · 2023Article
- HBZ upregulates myoferlin expression to facilitate HTLV-1 infection.PLoS pathogens · 2023Article
- Identification and characterization of a novel enhancer in the HTLV-1 proviral genome.Nature communications · 2022Article
- Regulation of HTLV-1 transformation.Bioscience reports · 2022Review
- Human T-Cell Leukemia Virus Type 1 Envelope Protein: Post-Entry Roles in Viral Pathogenesis.Viruses · 2022Review
- HTLV-1 intragenic viral enhancer influences immortalization phenotypeFrontiers in immunology · 2022Article
- The Past, Present, and Future of a Human T-Cell Leukemia Virus Type 1 Vaccine.Frontiers in microbiology · 2022Review
- Tuning Rex rules HTLV-1 pathogenesis.Frontiers in immunology · 2022Review
- Novel perspectives on antisense transcription in HIV-1, HTLV-1, and HTLV-2.Frontiers in microbiology · 2022Review
- HTLV-1 Infection and Pathogenesis: New Insights from Cellular and Animal Models.International journal of molecular sciences · 2021Review
- HTLV-1 bZIP factor: the key viral gene for pathogenesis.Retrovirology · 2020Review
63 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Natural antisense viral transcripts have been recognized in retroviruses, including human T-cell leukemia virus type 1 (HTLV-1), HIV-1, and feline immunodeficiency virus (FIV), and have been postulated to encode proteins important for the infection cycle and/or pathogenesis of the virus. The antisense strand of the HTLV-1 genome encodes HBZ, a novel nuclear basic region leucine zipper (b-ZIP) protein that in overexpression assays down-regulates Tax oncoprotein-induced viral transcription. Herein, we investigated the contribution of HBZ to HTLV-1-mediated immortalization of primary T lymphocytes in vitro and HTLV-1 infection in a rabbit animal model. HTLV-1 HBZ mutant viruses were generated and evaluated for viral gene expression, protein production, and immortalization capacity. Biologic properties of HBZ mutant viruses in vitro were indistinguishable from wild-type HTLV-1, providing the first direct evidence that HBZ is dispensable for viral replication and cellular immortalization. Rabbits inoculated with irradiated cells expressing HTLV-1 HBZ mutant viruses became persistently infected. However, these rabbits displayed a decreased antibody response to viral gene products and reduced proviral copies in peripheral blood mononuclear cells (PBMCs) as compared with wild-type HTLV-1-infected animals. Our findings indicated that HBZ was not required for in vitro cellular immortalization, but enhanced infectivity and persistence in inoculated rabbits. This study demonstrates that retroviruses use negative-strand-encoded proteins in the establishment of chronic viral infections.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.